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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

MAP/microtubule affinity-regulating kinase 3

MARK3, C-TAK1, Par-1A
The protein encoded by this gene is activated by phosphorylation and in turn is involved in the phosphorylation of tau proteins MAP2 and MAP4. Several transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Oct 2011] (from NCBI)
Top mentioned proteins: TAK1, MARK, cdc25, CAN, MARK4
Papers using MARK3 antibodies
Molecular mechanisms involved in Sertoli cell adaptation to glucose deprivation.
Lobaccaro Jean-Marc A., In PLoS ONE, 2008
... Anti-tubulin Yol1/34 antibody and rabbit anti-MARK3 was from Abcam.
Papers on MARK3
Atypical PKC phosphorylates microtubule affinity-regulating kinase 4 in vitro.
Hassan et al., New Delhi, India. In Mol Cell Biochem, Dec 2015
The interaction of MARK2 and MARK3 with aPKC and their negative regulation by aPKC is already known.
KA1-targeted regulatory domain mutations activate Chk1 in the absence of DNA damage.
Gillespie et al., Santa Cruz de Tenerife, Spain. In Sci Rep, 2014
Modelling indicates a high probability that this region of Chk1 contains a kinase-associated 1 (KA1) domain, a small, compact protein fold found in multiple protein kinases including SOS2, AMPK and MARK3.
Regulation of protein phosphatase 1I by Cdc25C-associated kinase 1 (C-TAK1) and PFTAIRE protein kinase.
Hemmings et al., New York City, United States. In J Biol Chem, 2014
We studied the effects of two protein kinases identified previously in purified brain PP-1I by mass spectrometry, Cdc25C-associated kinase 1 (C-TAK1) and PFTAIRE (PFTK1) kinase, for their ability to regulate PP-1I.
MARK4 and MARK3 associate with early tau phosphorylation in Alzheimer's disease granulovacuolar degeneration bodies.
von Euler et al., Södertälje, Sweden. In Acta Neuropathol Commun, 2013
MARK3 was localized to a subset of the GVD-containing neurons and also had a weak general cytoplasmic neuronal staining in both NDE and AD.
Genetic analysis of recently identified osteoporosis susceptibility genes in southern Chinese.
Tan et al., Hong Kong, Hong Kong. In J Clin Endocrinol Metab, 2013
We further demonstrated a significant interaction between MARK3 and serum ALP levels (Pmeta = 9.89 ×10(-6)); the effect of MARK3 rs11623869 on BMD was stronger in the presence of high serum levels of ALP.
The regulation and function of the NUAK family.
Zhao et al., Taipei, Taiwan. In J Mol Endocrinol, 2013
Twelve AMPK-related kinases (ARKs; BRSK1, BRSK2, NUAK1, NUAK2, QIK, QSK, SIK, MARK1, MARK2, MARK3, MARK4, and MELK) have been identified recently.
CBP501-calmodulin binding contributes to sensitizing tumor cells to cisplatin and bleomycin.
Kawabe et al., Numazu, Japan. In Mol Cancer Ther, 2011
CBP501 was originally described as a unique G(2) checkpoint-directed agent that binds to 14-3-3, inhibiting the actions of Chk1, Chk2, mitogen-activated protein kinase-activated protein kinase 2, and C-Tak1.
Discovery of cellular substrates for protein kinase A using a peptide array screening protocol.
Scott et al., Seattle, United States. In Biochem J, 2011
In the present paper we describe a strategy using peptide arrays and motif-specific antibodies to identify and characterize previously unrecognized substrate sequences for protein kinase A. We found that the protein kinases PKD (protein kinase D) and MARK3 [MAP (microtubule-associated protein)-regulating kinase 3] can both be phosphorylated by PKA.
Regulation of glucose homeostasis by KSR1 and MARK2.
Lewis et al., Omaha, United States. In Plos One, 2010
The kinase MARK2 is closely related to C-TAK1, a known regulator of KSR1.
TRESK background K(+) channel is inhibited by PAR-1/MARK microtubule affinity-regulating kinases in Xenopus oocytes.
Czirják et al., Budapest, Hungary. In Plos One, 2010
MARK1, MARK2 and MARK3 accelerated the return of TRESK current to the resting state after the calcium-dependent activation.
Loss of Par-1a/MARK3/C-TAK1 kinase leads to reduced adiposity, resistance to hepatic steatosis, and defective gluconeogenesis.
Piwnica-Worms et al., Saint Louis, United States. In Mol Cell Biol, 2010
Knockout mice were protected against high-fat diet-induced obesity and displayed attenuated weight gain, complete resistance to hepatic steatosis, and improved glucose handling with decreased insulin secretion.
OPG and RANK polymorphisms are both associated with cortical bone mineral density: findings from a metaanalysis of the Avon longitudinal study of parents and children and gothenburg osteoporosis and obesity determinants cohorts.
Tobias et al., Bristol, United Kingdom. In J Clin Endocrinol Metab, 2010
We also found suggestive evidence of an association between the MARK3 SNP (rs2010281) and BMDC but with a direction of effect opposite to that previously reported.
C-TAK1 interacts with microphthalmia-associated transcription factor, Mitf, but not the related family member Tfe3.
Mansky et al., Minneapolis, United States. In Biochem Biophys Res Commun, 2010
interaction between Mitf and C-TAK1 was demonstrated.
The regulation and function of mammalian AMPK-related kinases.
Carling et al., London, United Kingdom. In Acta Physiol (oxf), 2009
Recently, 12 AMPK-related kinases (BRSK1, BRSK2, NUAK1, NUAK2, QIK, QSK, SIK, MARK1, MARK2, MARK3, MARK4 and MELK) were identified that are closely related by sequence homology to the catalytic domain of AMPK.
New sequence variants associated with bone mineral density.
Stefansson et al., Reykjavík, Iceland. In Nat Genet, 2009
These are near the SOST gene at 17q21, the MARK3 gene at 14q32, the SP7 gene at 12q13 and the TNFRSF11A (RANK) gene at 18q21.
Conformational instability of the MARK3 UBA domain compromises ubiquitin recognition and promotes interaction with the adjacent kinase domain.
Pawson et al., Toronto, Canada. In Proc Natl Acad Sci U S A, 2007
identify a molecular mechanism through which the hMARK3 UBA domain has evolved to bind the kinase domain
Violating the splicing rules: TG dinucleotides function as alternative 3' splice sites in U2-dependent introns.
Platzer et al., Jena, Germany. In Genome Biol, 2006
occurrence of an unusual TG 3' splice site in intron 3
Opinion: alternative views of AMP-activated protein kinase.
Temple et al., Chapel Hill, United States. In Cell Biochem Biophys, 2006
Interestingly, the predicted protein structure of the carboxy-terminus of AMPKalpha resembles the carboxy-terminal KA-1 domain of MARK3, a Par-1 orthologue.
Solution structure of the kinase-associated domain 1 of mouse microtubule-associated protein/microtubule affinity-regulating kinase 3.
Yokoyama et al., Yokohama, Japan. In Protein Sci, 2006
Approximately 50 additional residues preceding the previously defined KA1 domain are required for MARK3 proper folding.
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